288 STEM END ROT OF MANGO IN AUSTRALIA: CAUSES AND CONTROL G.I. Johnson and A.W. Cooke, Plant Pathology Branch, Department of Primary Industries, Indooroopilly, Queensland 4068 A.J. Mead and I.A. Wells, Horticulture Branch, Department of Primary Industries, Ayr, Queensland 4807 Abstract Since 1986, over 6,000 mangoes cv. Kensington Pride from twelve locations in Queensland and one in the Northern Territory have been monitored for stem end rot development. Dothiorella dominicana has been the predominant cause of stem end rot at all sites. Lasiodiplodia theobromae (Syn. Botryodiplodia theobromae), Phomopsis mangiferae and other fungi (Dothiorella Mangiferae, Cytosphaeria mangiferae and other Dothiorella sp caused stem end rot much less frequently (<10% affected fruit), although a higher incidence of L. theobromae or P. mangiferae (30-40% of affected fruit) occurred at a few sites. At six of the Queensland sites, incidence of stem end rot on fruit from tagged trees has been monitored within and between seasons. Incidence was higher in older trees and in unsprayed trees. Possible sources of inoculum were assessed. D. dominicana was the main cause of twig dieback. The teleomorph of D. dominicana (Botryosphaeria sp.) was collected from dead twigs of mango found in leaf litter, Concurrent with studies on disease etiology and the seasonal severity of stem end rot, the effects of pre-and post-harvest fungicide treatments have also been examined. Pre- harvest sprays with copper oxychloride, iprodione or propiconizole reduced the incidence of stem end lesions. Post harvest treatment in hot benomyl provided good control of stem end rot caused by both D. dominicana and L. theobromae during storage at 20°C for 14 days. Hot benomyl followed by prochloraz provided effective control of stem end rot caused by D. dominicana and of alternaria rot (Alternaria alternata) during longer storage in a controlled atmosphere (3 weeks +) at 13°C. As trees in Australian plantations become older, the losses from stem end rot will increase. An integrated control program involving pre-and post-harvest control measures will be required to minimise losses. 1. Introduction Since the development of an effective control program for anthracnose (Colletotrichum gloeosporioides Penz.) in Australian mangoes, stem end rot has become the most significant cause of post harvest disease loss in Australia (Johnson et al., 1989). The term "stem end rot" has been used to describe disease lesions developing at the pedicel end of fruit after harvest. A range of symptoms can be observed, reflecting the fact that several pathogens can cause stem end rots. Acta Horticulticulturae 291, 1991 Mango289 Peterson (1984) reported that Dothiorella dominicana was the main cause of stem end rot in north Queensland mangoes, while Lasiodiplodia theobromae and Phomopsis mangiferae also caused the disease (Muirhead and Grattidge, 1984). L. theobromae is considered the main pathogen in other parts of the world (Peterson, 1984; Muller and Burt, 1989). Control measures developed for anthracnose have given only partial control of stem end rot (Muirhead and Grattidge, 1984). With the expansion of mango production in Australia, greater emphasis has been placed on control of stem end rot to extend shelf life in domestic and export markets. 2. Material and methods 2.1 Stem end rot survey In both the 1987/88 and 1988/89 seasons, five mango trees at each of six sites in north Queensland were tagged and sampled twice, two or three weeks apart, just prior to harvest. At each sampling, twenty fruit per tree were collected. At one site, during the second season, additional earlier samples were taken two weeks apart. Early-sample fruit were gassed with ethylene for 24 h and ripened at 25°C. Pulp dry matter was determined on five fruit from each sample. Stem end rot was assessed (% incidence) during storage for 20 days or until fruit became fully ripe. Isolations were made from all fruit affected by stem end rot. During the course of sampling, general observations were made about tree age, the amount of litter beneath the tree, adherence to pre harvest spray programs and watering regimes. To confirm pathogenicity and record sequential symptom development, a range of fungi ex mango were inoculated onto fruit after immersing them in hot water at 55°C for 5 mins to control latent infections which could have competed with the inoculum. As opportunity permitted, fruit affected by stem end rot from six other sites in Queensland, and one in the Northern Territory were sampled to determine the causes of the disease. 2.2 Sources of inoculum At two sites, the causes of twig dieback have been determined. Tree litter samples were collected at some sites and examined for the presence of stem end rot fungi. At one site, the fungi associated with foliar lesions were also identified. 2.3 Pathogen identification and in vitro growth Studies on the taxonomy of stem end rot fungi are currently underway (Johnson, unpublished). The cardinal temperature requirements for mycelial growth were determined for isolates of Dothiorella spp. and Lasiodiplodia theobromae by growing isolates on PDA in a multi-range incubator at temperatures from 10-40'C for 14 days.290 2.4 Fungicidal control During two seasons, pre-harvest fungicide sprays were evaluated to assess their effect on post-harvest disease. Fruit samples were treated with prochloraz (45EC, 0.55 ml/L, 30 sec) or left untreated prior to storage for two weeks (25°C) or four weeks (13°C) (Johnson et al., 1989; Peterson et al., 1989). Post harvest fungicides and hot water had been evaluated for control of stem end rot and other disease during storage at 25°C in air or at 13°C in a controlled atmosphere (5% 0, 5% CO,) (Johnson et al., 1989). es Results and Discussion 3.1 Stem end rot survey Dothiorella dominicana predominated as the cause of stem end rot at all sites (Johnson, unpublished). Data from some sites is shown in Figure 1. A higher level of Phomopsis mangiferae was observed at Delta Research Station, Bowen during the dry season (Table 1). Higher levels of Lasiodiplodia theobromae were recorded in two samples (Site 5, Mareeba and Katherine, N.T.). Notably, Cytosphaeria mangiferae Died. caused a few stem end lesions (Table 1). C. mangiferae also caused twig dieback (Table 4). Colletotrichum gloeosporioides and Aspergillus niger also caused lesions at the stem end in this survey. lesions caused by the latter two fungi were not classified as "stem end rot". At Ayr sites, levels of stem end rot on fruit, 14 and 20 days after harvest ranged from levels of stem end rot.on fruit, 14 and 20 days after harvest ranged from zero to 53% (Figure 2). At each site, stem end rot levels from samples within and between seasons were fairly consistent (Figure 3). The most severe stem end rot losses occurred on fruit froma site with mature trees that received no field sprays with fungicide in the first season. In addition, the trees were severely drought-stressed at the time of sampling (Ayr site 3, 1987). Higher levels of stem end rot also occurred at sites with older trees, especially where substantial litter had accumulated beneath the trees (Johnson, unpublished) . 3.2 Symptom production Dothiorella spp. and Lasiodiplodia theobromae produced similar symptoms, appearing as diffuse areas of water-soaked tissue radiating from the stem end in finger-like projections which quickly darkened and coalesced, giving lesions with wavy margins. The necrosis remained beneath the cuticle and penetrated the entire fruit within seven days or less at 25°C. Superficial mycelium appeared around the pedicel or through ruptures in the skin or, directly through the epidermis. A brown liquid leaked from the stem end or from surface ruptures. With D. dominicana and L. theobromae, pycnidia developed on the fruit surface, starting around the stem end. Fruiting body production was not observed with some other Dothiorella spp. (e.g. D. mangiferae).